Exposure to particulate air pollution is associated with increases in cardiovascular mortality and morbidity. The pathophysiological mechanisms underlying this observation are emerging, and exposure to particulate air pollution has been shown to result in increases in blood pressure and arterial tone, impaired vascular function and an increased tendency for blood to clot as well as an increase in atherosclerotic plaque burden. Recent evidence from panel studies and controlled exposure studies have suggested an increase in myocardial ischaemia (a reduction in blood flow to the heart) following exposure. In this study we aim to investigate directly myocardial (heart) blood flow following exposure to diesel exhaust (as a model of urban air pollution) using CT/PET myocardial perfusion imaging in male patients with stable coronary disease and healthy male controls. We hypothesize that following exposure to dilute diesel exhaust:

Myocardial blood flow will be reduced

Coronary flow reserve will be impaired

The magnitude of impairment will be higher in patients with coronary disease as compared to healthy controls

Coronary blood flow will be determined in the left anterior descending coronary artery using doppler echocardiography at rest and at peak adenosine stress 1 hour following exposure to diesel exhaust and filtered air

Healthy volunteers will be taking no regular medication, have a normal electrocardiogram and exercise stress test

Patients with a previous history of myocardial infarction or successful coronary revascularization (PTCA or coronary artery bypass grafting) but without symptoms of angina pectoris will be recruited

Exclusion Criteria:

Healthy volunteers:

Regular medication

Abnormal 12-lead electrocardiogram

Abnormal exercise stress test

Patients with coronary disease

Acute coronary syndrome within past 3 months

Impaired left ventricular function

Significant valvular heart disease

Left ventricular hypertrophy

Resting conduction defect

Digoxin use

Renal impairment (eGFR <60 mL/min)

Hepatic impairment

Asthma

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Please refer to this study by its ClinicalTrials.gov identifier: NCT01661582